척수손상 후 척수 내 ionotropic glutamate 수용기 활성화가 중추 신경병증성 통증 유발에 미치는 영향

Abstract

Background: Spinal cord injury (SCI) induces the development of central neuropathic pain which is characterized by symptoms such as allodynia, hyperalgesia, and spontaneous pain. However, the underlying mechanism is not fully understood. This study was conducted to see if activation of the glutamatergic system in the spinal dorsal horn is involved in the development of central pain following SCI. Methods: SCI was induced by a hemisection of the spinal cord at T13 in adult, male, Sprague-Dawley rats. Mechanical allodynia was tested by measuring paw withdrawal frequency in response to repeated applications of a von Frey hair to the plantar surface of the hind paw. Single neuronal activity of dorsal horn neurons (L4-L6) was recorded extracellularly using a carbon filament-filled glass microelectrode (2-4 Mℓ). The drugs were intrathecally and topically administrated on the spinal surface for behavioral and electrophysisological study, respectively. Results: After left spinal hemisection at T13, behavioral signs of mechanical allodynia developed on both hind limbs and the responsiveness of spinal dorsal horn neurons increased on both sides of the spinal dorsal horn. Ionotropic glutamate receptor antagonists including MK-801 (NMDA receptor antagonist) and NBQX (non-NMDA receptor antagonist) suppressed mechanical allodynia and increased responsiveness on both hind paws. Metabotropic glutamate receptor antagonist MCPG, however, had no significant effect. Conclusions: These results indicate that activation of the ionotropic, but not metabotropic, glutamatergic system in the spinal cord plays a key role in the development of central pain following SCI.